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Very cool new study on massage, from Mark Tarnopolsky’s group at McMaster (abstract here, press release here). Massage is one of those interventions that’s very difficult to study objectively — people like the feel of massage, you can’t blind them, and the outcomes you’re interested in are usually very subjective. But this study does a very good job.

The details: 11 volunteers exercised to exhaustion (about an hour or more on an exercise bike with gradually increasing pace) to induce muscle damage. Then, after a 10-minute break, one of their legs was massaged as follows:

The leg to be massaged was randomly selected, and no one except the massage therapist knew which leg had been massaged until after the results were analyzed.

So how to figure out what the massage did? They took three muscle biopsies from each leg: one at rest, one immediately after the massage, and one 2.5 hours after the massage. Then, because they didn’t know exactly what to expect, they did an untargeted whole-genome analysis to figure out which genes reacted differently between the massaged and non-massaged leg. The result:

[W]hen administered to skeletal muscle that has been acutely damaged through exercise, massage therapy appears to be clinically beneficial by reducing inflammation and promoting mitochondrial biogenesis.

How and why does this happen? The researchers suggest that “mechanical stretch or strain during massage treatment” activates the relevant signalling pathways. In fact, they suggest, the mechanism may be essentially the same as conventional anti-inflammatory drugs. Which is very cool. They also checked the rate of glycogen restoring and lactate clearance in the muscles; neither were improved by massage (which, in the case of lactate, we already knew).

So what does this tell us? Massage does something. Do these acute signalling changes translate to a clinically significant difference in muscle recovery a day later? Impossible to say for now. Is effleurage or petrissage more effective than one of those self-massage devices you can buy from late-night informercials, or than a foam roller? Who knows. But it’s a very good start.

One of the big challenges for researchers trying to figure out how to reduce post-workout muscle soreness is that it’s really hard to quantify that soreness. Asking someone “How sore are you?” is important, but highly susceptible to placebo effects; more objective measures like the enzyme creatine kinase (which is supposed to indicate muscle damage) now tend to be viewed as pretty unreliable proxies for muscle soreness. So how about this:

That’s an image from a new study that used an infrared camera to measure skin temperature before and after a series of biceps curls (press release here; freely available article and video in the Journal of Visualized Experimentshere). They suggest that skin temperature that remains elevated 24 hours after exercise indicate muscle damage:

This damage in the muscle causes additional heat transfer from the muscle to the overlying skin, which causes a detectable hot spot under the skin.

And sure enough, their study did find elevated skin temperature in the biceps (33.96 C instead of 32.80 C) 24 hours after exercise. The problem is that the temperature returned to normal (32.82 C) after 48 hours. The subjects’ subjective assessment of soreness, on the other hand, was equally elevated after 24 and 48 hours — so clearly skin temperature isn’t a perfect proxy for what we experience as soreness. Still, it could be an interesting way for researchers to look at the early stages of delayed-onset muscle soreness in a quantifiable way. And it makes pretty pictures.

The subjects in the study did eight weeks of heavy weight training — using only one leg (their dominant one). As you can see, they dramatically increased strength in both legs. This effect is well known, but I still think it’s pretty cool! The goal of this particular study was to try to figure exactly how this happens, using magnetic pulses to the brain to help assess the role of the nervous system. They did indeed find a significant reduction in “corticospinal inhibition” in both legs, suggesting that the training improves the transmission of the signal from the brain to the muscle, and this improvement applies to both sides of the body.

The point? Well, as the researchers note, it’s something to bear in mind if you have an injury in one leg or one arm. You might be able to keep the injured limb strong without even exercising it. Of course, you have to balance that against the risk of creating physical imbalances. I guess the ideal would be to train enough to increase strength without actually putting on muscle. As the researchers conclude, clinical trials of this approach are needed.

When infection occurs, neutrophils rapidly migrate to the infection site (chemotaxis) and ingest the pathogens (phagocytosis).

So how does exercise affect these neutrophils? Well, that depends on what kind of exercise you do. For regular, moderate exercise (“CME,” or “chronic moderate exercise,” consisting of 30 minutes of moderate cycling daily for two months), here are the results:

“DT” is “detraining.” So you can clearly see that regular, moderate exercise boosts the ability of the neutrophils to get to infection sites quickly (chemotaxis) and attack the bad guys (phagocytosis). And in fact, the neutrophils are still ultra-alert for a couple of months after you stop training. In addition, the researchers found that regular exercise extended the life of the neutrophils.

On the other hand, the effects of “acute severe exercise” (an incremental test to exhaustion) had more mixed results. Chemotaxis was enhanced, but phagocytosis wasn’t, and the lifespan of the neutrophils was shortened — not so good for immune function.

So is this a surprise? Not really — it’s been clear for a long time that exercise has a J-shaped influence on immune function. Some is good, more is better, but beyond a certain point, too much is bad. Run a marathon, you’ll have a slightly elevated risk of catching a cold (or at least suffering from some sort of respiratory symptoms) afterward. But studies like this are needed to understand what exactly is happening in the body, so that eventually we’ll have a better idea of exactly where the curve in the J starts — and possibly figure out some ways to extend the sweet spot of the curve.

The good news: Sidney Crosby is back from the concussions that kept him on the bench for more than 10 months, and he had two goals and two assists in his return against the Islanders last night. But one downside, a reader pointed out to me in an e-mail, is that Crosby’s return may give added credibility to “chiropractic neurology,” the alternative therapeutic approach that Crosby turned to during his rehab. What exactly is this? I don’t know — and I’m not alone:

It’s a field that’s unfamiliar to many traditional doctors, including Randall Benson, a neurologist at Wayne State in Detroit who has studied several ex-NFL players. Says Benson, “It’s very difficult to evaluate what kind of training, expertise or knowledge a chiropractic neurologist has since I have never heard of [the discipline].”

In 1998, at Parker University, a Dallas chiropractic college, Carrick [the chiropractic neurologist who Crosby worked with] worked on Lucinda Harman before 300 students. Two car accidents and a neurotoxic bite from a brown widow spider had left Harman, herself a Ph.D. in experimental psychology, wheelchair-bound and with headaches, during which she saw spots.”[Carrick] asked if they were red and yellow,” she says. “I said, ‘No, they’re green, blue and purple.’ ” Carrick informed the audience that this meant her brain was being drastically deprived of oxygen and that, without treatment, she had six months to live. Harman, now 59, says simply, “Miracle.” But Randall Benson says that “there’s nothing out in peer-reviewed literature supporting” an association between the color of spots a patient sees during a headache and the severity of the oxygen deprivation in the brain.

[...]

Carrick, who has had a handful of studies that have appeared in scientific journals, has never published data on vestibular concussions. “We don’t have enough time to publish studies,” he says, “but we’re doing a large one at Life [University] right now.”

It’s a great piece — fair but rigorous. In some ways, though, the most important quote may be the kicker:

“I don’t think this is a case of trying to do something wacky,” Crosby says. “When someone came along and invented the airplane, people must have thought they were out of their mind. Who thinks he can fly? I’m sure people thought that person might have been stretching it a bit… . At the end of the day, as long as the person getting the care is comfortable, I think that’s what’s important.“

Much as my evidence-based personality protests, I do think there’s some truth to that. Especially in cases like this, where — as with so many health conditions — there isn’t a well-established “standard-of-care” treatment. It’s totally different from, say, Steve Jobs choosing “alternative” forms of cancer treatment instead of surgery. In that case, the potential benefits of the surgery are well-known and well-understood. But many people face health conditions where the verdict of the Cochrane review is basically “there is insufficient evidence to conclude that ANY interventions do any good.” In that case, it’s hard to argue against trying other, unproven approaches rather than simply doing nothing.

Of course, sports medicine is a little different — it’s not life-or-death. For pro athletes, the incentive to try anything and everything in order to return to play (and earn money during their brief career window) is enormous. If I were Tiger Woods or Terrell Owens, I would have tried platelet-rich plasma to speed tendon healing too, despite the lack of evidence that it actually works. The problem is that the use of these therapies by sports stars gives the general public the impression that they’re proven, established treatments — hence the huge surge in PRP over the last few years. Will the same thing happen with chiropractic neurology? I hope not. But on the other hand, if someone who’s been in two car accidents and been bitten by a neurotoxic spider is in pain and hasn’t been able to get relief from conventional treatment, I’d have a hard time criticizing them if they decided to give it a try.

My Jockology column in today’s Globe and Mail takes a look at the paleo diet — or rather, the paleo “lifestyle.” The column is actually in the form of an infographic in the paper, beautifully illustrated as “cave art” by Trish McAlaster. Unfortunately, the online version so far just lifts the text, without any of the data and graphics that accompany it. Nonetheless, it’s hopefully worth a read!

As a teaser, here’s an excerpt from a section on how the pace of evolution has changed over the past few thousand years, and what that means for the quest for the perfect “ancestral” diet:

The paleo diet depends on the assumption that our genes haven’t had time to adapt to the “modern” diet. Since evolution depends on random mutations, larger populations evolve more quickly because there’s a greater chance that a particularly favourable mutation will occur. As a result, our genome is now changing roughly 100 times faster than it was during the Paleolithic era, meaning that we have had time to at least partly adapt to an agricultural diet.

The classic example: the ability to digest milk, which developed only in populations that domesticated dairy animals. More than 90 per cent of Swedes, for example, carry this mutation. Finnish reindeer herders, in contrast, acquired genes that allow them to digest meat more efficiently, while other populations can better digest alcohol or grains. The “ideal” ancestral diet is most likely different for everyone. [READ THE WHOLE ARTICLE]

And, as another teaser, here’s a section of Trish’s infographic illustrating the difference between the acute stress of the paleo lifestyle compared to the chronic stress of modern life:

Ice baths after a hard workout are very popular, but the evidence for them has always been a little shaky. A group of British researchers (including a pair from the English Institute of Sport) have just published a major meta-analysis in the British Journal of Sports Medicine that adds a couple of interesting insights. The analysis covers 14 different studies with a total of 239 athletes.

What I found most interesting is the following distinction they decided to make:

For the purpose of this review, exercise will be subdivided into two categories: ‘eccentric exercise’ that refers to the stress caused from exercise incorporating high mechanical stress (eg, eccentric contractions) and ‘high-intensity exercise’ that refers to stress caused from exercise with a high metabolic cost as well as some elements of eccentric muscle contractions (eg, repeat sprint sports).

It’s well known that the best way to induce muscle soreness is with eccentric muscle contractions, particularly unfamiliar ones. So most lab experiments on muscle soreness involve simple things like lowering a dumbbell or stepping off a box over and over — it may not be exhausting, but it sure leaves you sore. The problem is, this isn’t the kind of damage that most athletes are interested in recovering from — they’re interested in recovering from training sessions that feature familiar but intense exercise.

So is there a difference between the two? Yes: the meta-analysis found dramatically stronger effect on recovery from “high intensity exercise” than from “eccentric exercise.” It’s worth noting that only two studies looked at the former, while 12 looked at the latter. Still, it offers a possible explanation for why so many athletes believe ice baths help them in training, while lab studies of eccentric exercise continue to find ambiguous results.

Speaking of results, what were the overall conclusions? I quite like the use of forest plots to give a quick visual sense of the overall data. Here are the results for perceived recovery from muscle soreness, with each dot representing a study result (some studies appear more than once for results at 24, 48, and 72 hours after exercise, which is why there are more than 14 dots). Dots to the right of the thick line mean that the ice bath group recovered more quickly; dots to the left of the line indicate that the control group recovered more quickly:

Looks pretty convincing, eh? Unfortunately, the picture is a bit muddier if you look at an objective measure like creatine kinase in the blood (a marker of muscle damage), though there’s still a statistically significant effect in favour of ice baths:

Same goes for recovery of strength:

In the end, we’re still plagued by the fact that it’s impossible to placebo-control an ice bath study. The perceived soreness results do look encouraging, but it’s hard to rule out the effects of the fact that most of the subjects probably expected to feel better when they had the ice bath. By no means is the science settled here yet.

Which brings us to another point that’s currently being hotly debated in scientific and athlete circles (as commenter Rich pointed out last time I blogged about ice baths): If inflammation is part of the body’s adaption response to stress, and ice baths reduce inflammation, does that mean ice baths reduce your adaption to hard training? Interestingly, the lead author of the current study, Jonathan Leeder of the English Institute of Sport, commented on this question in an EIS press release last year:

“There’s evidence to suggest that if you constantly decrease the stress in training that the body won’t adapt, so long term use of a recovery technique, such as an ice bath, should be reviewed to avoid any detrimental effects on performance and to ensure that these techniques have their biggest impact when needed during competition” [Leeder] adds.

But is there really evidence to back this hypothesis up? Here’s what Leeder and his co-authors say in the peer-reviewed BJSM:

It has, however, been suggested that the inflammatory response is critical for optimal repair of damaged tissue. Although the mechanisms of training adaptation are not fully understood, it may be detrimental to reduce the commonly accepted damage-repair-adaptation model by diminishing the inflammatory response; however, there is a lack of evidence to support this. This raises the question of whether frequent or habitual use of strategies designed to reduce inflammatory responses can be detrimental for elite athlete adaptation to training.

So that’s where we’re at: no one really knows whether repeated ice baths have a practically significant effect on reducing adaption to training. From what I understand, the English Institute of Sport has been advising its athletes to avoid ice baths after routine sessions during heavy training phases, but to incorporate them during tapering and competition. In other words, periodize your recovery protocols so that you maximize adaption during training periods and maximize recovery during competition periods. Does this work? Maybe we’ll find out at next year’s Olympics!

[...] Patients “see a high-profile athlete and say, ‘I want you to do it exactly the same way their doctor did it,’ ” said Dr. Edward McDevitt, an orthopedist in Arnold, Md., who specializes in sports medicine.

The result is therapies that are unproven, possibly worthless or even harmful. There is surgery, like a popular operation that shaves the hip bone to prevent arthritis, that may not work. There are treatments, like steroid injections for injured tendons or taping a sprained ankle, that can slow the healing process. And there are fads, like one of Ms. Basle’s treatments, P.R.P., that soar in popularity while experts debate whether they help.

All this leads Dr. Andrew Green, a shoulder orthopedist at Brown University, to ask, “Is sports medicine a science, something that really pays attention to evidence? Or is it a boutique industry where you have a product and sell it?”

“For a lot of people it is a boutique business,” he said. “But are you still a doctor if you do that?”

The article focuses on platelet-rich plasma (PRP) therapy, since it’s a perfect example of the hype-before-evidence phenomenon that’s so common in sports medicine. Kolata discusses the mishmash of conflicting evidence, and the reasons the treatment seems plausible. But she also points out the inevitable conflicts of interest from some of the scientists whose evidence is used to support PRP:

They included Dr. Allan Mishra, an orthopedist in private practice in Menlo Park, Calif., who is supported by and gets royalties from one of the P.R.P. equipment makers, Biomet, and is on the board of directors and owns stock in another company, BioParadox, which is exploring the treatment for cardiovascular disease.

Dr. Mishra says more research is needed but offers the treatment for a variety of injuries. His Web page includes a TV news video that claims P.R.P. cured a Stanford football player, James McGillicuddy, with a torn knee tendon. On the program, Dr. Mishra says that, in general, 90 percent of the patients he treats “get better and stay better” after the treatment.

Wow, 90 percent success rate! Too bad he didn’t publish those results, because that’s not what any of the studies say. It sounds more like he “has a product and is selling it” — and unfortunately, that’s all too common with “breakthroughs” in sports medicine and physiotherapy.

Athletes have to fly to competitions — it’s an inevitable part of international sport. But flying long distances can hurt performance. There are lots of “rules of thumb” that people use to plan travel and competition (e.g. allow one day of recovery for each time zone crossed), but not a lot of hard evidence. Australian researchers have just published a neat study in the European Journal of Applied Physiology that sheds a little light on this question.

The study looked at five members of the Australian skeleton team before and after a flight to a training camp in Canada that took 24 hours and involved four different flights (so a pretty brutal travel schedule, but not that rare for athletes). Two days before they left, they did a bunch of power tests: box drop jumps, squat jumps, and countermovement jumps. Once they arrived in Canada, they repeated these measurements daily for 11 days. Some Canadian skeleton athletes (who didn’t have to fly) also did some of the tests as a control.

The data, frankly, is pretty messy. Performance clearly drops after the flight, but the various measurements aren’t perfectly consistent about when the biggest drops come and how quickly performance returns. Here’s a bit of sample data, showing the squat jump height. The two squares (instead of circles) are the Canadian controls — they basically just show that there’s not much day-to-day variation in the measurements for non-jetlagged athletes:

So what’s going on? The researchers believe that it’s not just being cooped up in a plane for a day that causes the problems:

We would contend that a symptom of jet lag is circadian misalignment and as such the performance declines that we are reporting are the result of circadian misalignment due to trans-meridian flight.

Seems fairly reasonable. The solution:

This research highlights that where possible, athletes performing explosive short duration efforts as part of a competitive environment should time their arrival in the destination country following long haul travel at least five days prior to the competition.

This I’m a little more skeptical about. Looking at the data, it’s hard to see any particular break point after five days. That being said, in the balance between leaving too little time to recover versus arriving too early and being out of your element for too long, five days does seem like pretty good common sense.

Just last week, I posted about the first serious study on the use of “cryosaunas” for post-workout recovery. Now I have an important update for athletes considering using a cryosauna: make sure to take off any sweaty clothes before you enter the sauna! According to AP, Justin Gatlin, the 2004 Olympic champion sprinter (and convicted doper), has arrived in South Korea for the World Championships sporting a serious case of frostbite caused by wearing sweaty socks into a cryosauna:

“You wake up at 9 o’clock in the morning in Orlando and it’s already 90 degrees,” said the 29-year-old Gatlin, who lives and trains in Florida. “So we’re already hot, drenched with sweat. Get in the booth, socks were wet, socks froze to me instantly.”

[...] Gatlin said the pain from the frostbite had subsided and the injury hadn’t affected his stride. But it is still bothersome because the wounds on his heels are near the level where his socks sit and where the back of his running spikes touch.

“It’s better than it was. It was all pussed up and blistered. It bubbled up and it stayed bubbled up for a good four or five days,” Gatlin said, lifting up his sweat pants to reveal the scabby scars that resemble big blisters.

So there you go: using liquid nitrogen for post-workout recovery has some downsides. Who knew?